The life cycle of Caenorhabditis elegans contains a developmentally arrested state called dauer that occurs in response to adverse environmental conditions. This dauer stage is a period of prolonged cellular quiescence that is associated with not only the maintenance but also reprogramming of the Vulval Precursor Cells (VPCs) into a multipotent state. Normally in development, VPC fate specification requires LIN-12/Notch, a well- conserved transmembrane receptor and transcriptional activator, for transcriptional activation of target genes to define the future cell identity. However, during dauer, this transcriptional activation is blocked, even in the presence of a stable and activated LIN-12/Notch. Moreover, VPCs that had already undergone cell fate specification by LIN-12/Notch are de-differentiated into a multipotent state upon dauer entry. This block is mediated by Insulin/Insulin Growth Factor Signaling, as loss of its effector, the transcriptional factor DAF- 16/FoxO, results in a partial relief of the block. To study how dauer VPCs are able to prevent LIN-12/Notch signaling, I will investigate how LAG-1, the DNA-binding component of the LIN-12/Notch activation complex, is regulated in dauer VPCs, and I will test whether expressing stable and functional LAG-1 will relieve the dauer block. I will also perform a differential gene expression analysis experiment between blocked and unblocked dauer VPCs to look for candidates that may prove essential for maintaining VPCs in a quiescent and multipotent state.